Category: Understand why

  • What Are the Causes of Angina ?

    What Are the Causes of Angina ?

    Overview

    Angina is often described as a tightness or pressure in the chest, jaw, or arm, that happens when your heart muscle isn’t getting enough oxygen-rich blood. This lack of oxygen is called myocardial ischemia. Understanding What Are the Causes of Angina helps in recognizing and managing this condition.

    The most common cause of angina is a narrowing of the heart’s own blood vessels, known as the coronary arteries. However, there are also other, less common causes that can lead to your heart muscle not getting the blood supply it needs.

    In Details

    • Coronary Atherosclerosis (the most frequent cause).
    • Other Coronary Artery Diseases: These include blockages (emboli), sudden artery tightening (spasm), blood vessel inflammation (vasculitis), Kawasaki disease, and heart/vessel birth defects (congenital anomalies).
    • Cardiac Diseases: Such as a thickened heart muscle (hypertrophic cardiomyopathy), very high blood pressure (severe hypertension), or issues with a major heart valve (severe aortic valve disease).
    • High Output States: Conditions where the body’s demand for blood is unusually high, like severe anemia (low red blood cell count) or an overactive thyroid gland (thyrotoxicosis).

    The usual underlying problem causing this is coronary atherosclerosis. This is a common and progressive disease where plaques, which are fatty deposits, build up inside the walls of the coronary arteries. These arteries are crucial because they are responsible for supplying oxygen-rich blood directly to the heart muscle itself. As these plaques accumulate, they narrow the arteries, making it much harder for sufficient blood to reach the heart, especially when the heart has to work harder, such as during exercise, emotional stress, or exposure to cold temperatures.

    It’s important to know that while coronary atherosclerosis is very common, its presence doesn’t always result in angina. However, when it does, it’s a clear sign that the narrowed arteries are struggling to meet the heart’s oxygen demands, leading to the characteristic discomfort of angina.

    Beyond atherosclerosis, other, less common conditions can also lead to angina. These can involve other diseases that directly affect the coronary arteries themselves, such as emboli (small blood clots or other material that travel through the bloodstream and can block an artery), spasm (a sudden, temporary tightening of the artery walls that restricts blood flow), or vasculitis (inflammation of the blood vessels). Very rare conditions like Kawasaki disease (which primarily affects children and can cause inflammation of blood vessels) or congenital anomalies (structural problems with the heart or its blood vessels that are present from birth) can also be underlying causes.

    Furthermore, angina can result from other heart conditions that put an excessive strain on the heart, even if the coronary arteries are not primarily narrowed by atherosclerosis. For instance, hypertrophic cardiomyopathy is a condition where the heart muscle becomes abnormally thick, making it harder for the heart to pump blood effectively and potentially leading to oxygen deprivation. Similarly, severe hypertension (very high blood pressure) and severe aortic valve disease (a problem with one of the heart’s major valves) can significantly increase the heart’s workload, causing it to demand more oxygen than it can receive, thereby triggering angina.

    Lastly, conditions known as high output states can cause angina because they force the heart to work exceptionally hard to pump enough blood around the body. Examples include severe anemia, and thyrotoxicosis ( an overactive thyroid gland that speeds up the body’s metabolism and places a greater demand on the heart ).

    Other similar questions

    What is angina?

    Angina pectoris is a clinical syndrome of discomfort, typically felt as a pressure, tightness, or discomfort in the chest, jaw, arm, or other areas, that occurs when your heart muscle isn’t getting enough oxygen-rich blood

    Can you have coronary artery disease without experiencing angina?

    Yes, absolutely. It is possible to have coronary atherosclerosis (fatty deposits in the arteries) without any symptoms of angina when having atherosclerotic plaques that don’t cause stenoses( narrowing of the coronary arteries ). Also, myocardial ischemia (lack of blood flow to the heart) can occur without pain, a condition known as ‘silent ischemia’ which is more common in elderly patients and those with diabetes mellitus.

    Can other things cause chest pain that isn’t angina?

    Yes, there are many other causes of chest pain that are not related to angina. These can include problems with your lungs (like pneumonia or pulmonary embolism), issues with your digestive system (like esophagitis or a peptic ulcer), or even problems with your chest wall (such as muscle strains or costochondritis). Sometimes, psychological factors can also contribute to chest pain. So, it’s very important to differentiate between cardiac angina and other non cardiac causes of chest pain.

    Resources

    Clinical presentation and diagnosis of coronary artery disease: stable angina
    S W Davies Department of Cardiology, Royal Brompton Hospital, London, UK

  • What causes a blood clot in Coronary Heart Disease?

    What causes a blood clot in Coronary Heart Disease?

    Hello there, whether you’re a patient, someone who knows a patient, or just looking to understand more about heart health, let’s discuss What causes a blood clot in Coronary Heart Disease

    Overview

    When we talk about serious events like a heart attack, a blood clot forming in one of the heart’s arteries (coronary arteries) is almost always the cause. This isn’t just a random event; it’s typically triggered by something happening within the artery wall itself: the disruption of an atherosclerotic plaque. Imagine the artery wall as having a delicate inner lining. When this lining, where a fatty plaque has built up, gets damaged or cracks, the material inside the plaque gets exposed to the blood flowing by.

    This exposure acts like an emergency signal, causing blood cells called platelets to rush to the site and become sticky, and also activating the blood’s natural clotting system. This rapid response is normally meant to stop bleeding, but in the artery, it can quickly lead to the formation of a large blood clot that blocks the artery, cutting off blood flow to part of the heart muscle. This process involves a complex interplay between the “solid” components exposed from the plaque and the “fluid” components within your blood.

    In Details

    A condition called Acute coronary syndrome happens, and here we are about to know what triggers it and how does it start with the formation of the clot.

    Let’s have a quick look at what happens first

    • Physical disruption of an atherosclerotic plaque (e.g., rupture of its fibrous cap, superficial erosion).
    • Exposure of collagen from the plaque’s extracellular matrix to the blood.
    • Activation and aggregation of platelets.
    • Exposure of Tissue Factor (TF) from within the plaque.
    • Activation of the coagulation cascade.
    • Formation of a platelet-fibrin blood clot (thrombus).
    • Influence of “fluid-phase” blood factors, such as high levels of Plasminogen activator inhibitor-1 (PAI-1).

    Acute coronary syndromes, such as heart attacks, are overwhelmingly caused by the physical disruption of an atherosclerotic plaque within a coronary artery. This disruption can take several forms, most commonly a tear or rupture in the plaque’s protective fibrous cap. Less frequently, it can be due to superficial erosion of the artery lining, bleeding within the plaque itself (intraplaque hemorrhage), or the erosion of a calcified nodule. When any of these disruptions occur, the inner contents of the plaque, which are highly reactive, are suddenly exposed to the flowing blood.

    This exposure immediately triggers a cascade of events at a molecular and cellular level. First, contact with collagen from the exposed extracellular matrix of the plaque causes platelets to rapidly activate and stick to the site. Platelets are tiny blood cells crucial for blood clotting. Simultaneously, Tissue Factor (TF), a powerful pro-clotting protein produced by macrophages (a type of immune cell) and smooth muscle cells within the plaque, is also exposed.

    This Tissue Factor initiates the coagulation cascade, a complex series of chemical reactions that leads to the formation of thrombin. Thrombin then plays a dual role: it not only further amplifies the activation of platelets but also converts a blood protein called fibrinogen into fibrin. The activated platelets also release von Willebrand factor. Together, fibrin and von Willebrand factor act as molecular “glue,” forming a dense, three-dimensional network that traps more platelets and other blood cells, quickly building up a “white” arterial thrombus (blood clot).

    Beyond the direct “solid-state” triggers from the plaque itself, the “fluid phase” of your blood also plays a role in how likely a clot is to form and persist. For example, higher circulating levels of Plasminogen activator inhibitor-1 (PAI-1) can predispose you to clotting. PAI-1 reduces your body’s natural ability to break down clots, meaning any clot that forms is more likely to grow larger and last longer. Conditions like diabetes and obesity can increase PAI-1 levels, and hormones associated with high blood pressure can also boost its expression. This interplay between the “vulnerable plaque” and a “vulnerable patient” (due to blood factors) determines the risk of a cute coronary syndrome.

    Other Similar Questions

    What makes a plaque “vulnerable” to rupture?

    Vulnerable plaques are typically characterized by a thin, fragile fibrous cap (the protective outer layer), a large, soft lipid (fatty) core, and many inflammatory cells while having fewer smooth muscle cells that help strengthen the cap.

    Do only large blockages cause clots?

    No, many dangerous blood clots form at sites of plaques that do not cause significant narrowing (non stenotic lesions). These “hidden” lesions can have large fatty cores and thin caps, making them prone to rupture and causing a heart attack even if they haven’t caused any symptoms or noticeable blockages beforehand.

    Is it just one problem spot in the arteries?

    Not necessarily. While an acute event might stem from one “culprit lesion,” research shows that patients with acute coronary syndromes often have multiple disrupted plaques throughout their coronary arteries, and the underlying inflammation is often widespread, not just limited to one area.

    Resources

    For more detailed information, you can refer to the source document:

    • Libby, P., & Theroux, P. (2005). Pathophysiology of Coronary Artery Disease. Circulation, 111(25), 3481–3488.